Based on our findings that BACE2 proteolytically cleaves hIAPP at residues F15 and F23, one may predict BACE2 therapy as means for disrupting both IAPP-IAPP and IAPP-Aβ interactions at a molecular level and, in so doing impede homo- and hetero-amyloidosis. The gene discussed is IAPP; the disease is amyloidosis.